链脲佐菌素诱导糖尿病大鼠心肌缺血／再灌注损伤

Myocardial ischemia reperfusion injury in STZ-induced diabetic rats

目的研究链脲佐菌素(STZ)诱导的糖尿病大鼠缺血/再灌注(I/R)心肌的损伤,从心电图、心肌梗死面积、心肌大体和超微结构观察损伤的程度并分析其可能的作用机制。方法采用STZ(45 mg/kg)诱导大鼠糖尿病4周后制备心肌缺血30 min再灌注120 min模型,连续检测心电图变化,用2,3,5-氯化三苯基四氮唑(TTC)染色法测定心肌梗死面积、HE染色和电镜下观察心肌组织结构的改变。结果糖尿病大鼠由I/R损伤引起的心肌梗死面积并没有增加,但是HE染色和电镜下均发现糖尿病心肌损伤更为严重,肌纤维结构消失、心肌细胞膜和细胞核损伤、线粒体降解、血管淤滞、内皮损伤。结论 STZ诱导糖尿病4周的大鼠缺血/再灌注后心肌损伤较非糖尿病大鼠加重。

Objective To observe the myocardial ischemia-reperfusion injury in STZ-indueed diabetic rats, and to explore its mechanism on ECG, myocardial infarct size and morphology. Methods Diabetic rats were subjected to myocardial injurg by 30 rain of myocardial ischemia and 120 rain of reperfusion. At four weeks after STZ-induced diabetes, ECG was monitored constantly. Myocardial infarct size was measured by using the staining agent 2,3,5-triphenyltetrazolium chloride（TTC）. The changes of myocardial morphology were examined by light and electron microscopes. Results Compared with nondiabetic rats, the myocardial infarct size of diabetic rats induced by ischemia-reperfusion did not enlarge. However, the abnormal myocardial morphology were significantly more serious, including the disappearance of special structure of myofilaments, injury of cardiomyocyte membrane and nucleus, degradation of mitochondria, obstruction of blood vessels, and injury of endothelium. Conclusions The myocardial ischemia-reperfusion injury in STZ-induced diabetic rats is more serious than in non-diabetic rats.